Principal Investigator

We investigated urate excretion mechanism at human intestine and kidney in the present research. We therefore collected many cases including acute gastroenteritis and inflammatory bowel disease, as well as hemodialysis (end-stage renal disease) patient to compare healthy controls. As results, dysfunction of transporter ABCG2 significantly elevated serum uric acid (SUA) level in acute gastroenteritis patients regardless of the degree of dehydration, which was not detected in their recovery period. Furthermore, ABCG2 dysfunction also significantly increased SUA levels in hemodialysis patients. Thus, urate, which is excreted from both intestine and kidney, is elevated in both acute gastroenteritis and hemodialysis by dysfunctional ABCG2 variants. Also, it was implied that increased SUA could be a useful marker not only for dehydration but also epithelial impairment of intestine.